Biomedicine & Pharmacotherapy (May 2022)

Recombinant P40 protein of Schistosoma japonicum inhibits TREM-1 expression in RAW264.7 cells via FOXO3a

  • Pei Shen,
  • Tianyu Zhang,
  • Guo Chen,
  • Bei Zhang,
  • Ailong Huang,
  • Lian Duan,
  • Dandan Zhu,
  • Jinling Chen,
  • Jianxin Wang,
  • Yinong Duan

Journal volume & issue
Vol. 149
p. 112826

Abstract

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Triggering receptor expressed on myeloid cells 1 (TREM-1) is a transmembrane glycoprotein receptor and TREM-1 expression reached the peak at 6 weeks after infection with Schistosoma japonicum and inhibited subsequently. Since TREM-1 may be involved in the macrophage polarization process, the reason for the inhibition of TREM-1 expression in chronic schistosomiasis engaged us in them. In this study, flow cytometry was used to observe TREM-1 expression in peritoneal macrophages from mice infected with Schistosoma japonicum. Since P40 is one of the main components from schistosoma eggs, western blot and dual-luciferase reporter assays were performed to observe the effect of recombinant Schistosoma japonicum P40 protein (rSjP40) on TREM-1 expression in the mouse leukemic monocyte/macrophage cell line RAW264.7. These methods were also conducted to observe the effect of FOXO3a on the expression of TREM-1 in RAW264.7 cells, and a ChIP assay was performed to confirm the binding site of FOXO3a to the TREM-1 promoter. Our results showed that TREM-1 expression reached the peak in peritoneal macrophages from mice at 6 weeks after infection with Schistosoma japonicum. rSjP40 inhibited TREM-1 promoter activity at the position of − 1924 ~ − 1531 bp. rSjP40 down-regulated TREM-1 and FOXO3a protein expression in RAW264.7 cells. TREM-1 protein expression may be regulated by binding of FOXO3a to the promoter of TREM-1 in RAW264.7 cells. In conclusion, we found that rSjP40 inhibited TREM-1 expression in macrophages by inhibiting FOXO3a expression. This study will provide the basis for the study to explore the role of TREM-1 in Schistosoma japonicum infection.

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